Osteoprotegerin Human ELISA

Product specifications for - Osteoprotegerin Human ELISA

Overview:
Product group:	Assays
Category:	ELISA / EIA

Properties:
Molecular weight:	120 kDa
Assay Sensitivity:	0,03 pmol/l
Assay Precision:	Inter assay: n = 3, CV = 5,8%, Intra assay: n = 8, CV = 3,5%,
Assay Sample Type:	serum and plasma (EDTA, citrate, heparin)
Assay Time:	The total assay time is less than 3.5 hours
Assay Detection Range:	1,5 - 60 pmol/l
	IVD Certification
UNSPSC:	41116158
Storage instructions:	Store the kit at 2-8-¦C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Scientific information:
Scientific info:	Osteoprotegerin (OPG, osteoclastogenesis inhibitory factor, OCIF) is a product of the TNFRSF11B gene, located on chromosome 8q24. OPG belongs to the TNF (tumor necrosis factor receptor) superfamily, that plays a key role in bone remodeling. Human OPG is a secreted glycoprotein composed of 401 aminoacid residues. OPG exists as a disulfidelinked homodimer (120 kDa) or as a monomer (60 kDa). Both of these forms are active but the dimer is more bioactive than the monomer. In contrast to most members of the TNF receptor superfamily, OPG probably exists only in a soluble form. Its ligands are RANKL and TRAIL. Human OPG shares 85% aminoacid identity to mouse OPG and 86 % identity to rat OPG. In adult humans OPG mRNA is highly expressed in bones (osteblasts), endothelial vessel cells, skin, liver, stomach, intestine, heart, brain and lung and is also present in atherosclerotic plaques. OPG and RANKL are involved in bone resorption and bone formation. OPG and receptor RANK compete with each other for binding to the ligand RANKL. Binding of RANKL to RANK stimulates osteoclasts and their activity. When RANKL binds to OPG, osteoclastogenesis decreases. OPG prevents the formation of RANKL/RANK, inhibits formation of osteoclasts and suppress bone resorption. At normal physiological conditions OPG and ligand RANKL are in balance and bone resorption and bone formation are linked. This balance can be disrupted by the lack of estrogens in menopausal women, by anti-inflammatory effect of cytokines and by changes in the level of glucocorticoids, thyroid hormones, parathyroid hormone or calcitriol. Any modification in the RANKL/OPG ratio can induce either excessive bone resorption or, in contrast, excessive bone formation. This disregulation can lead to pathological conditions such as osteoporosis/osteopenia, bone tumor associated osteolysis, or cardiovascular pathology. In postmenopausal osteoporosis, OPG serum level decreases and this decrease can be an indicator of a higher risk for bones fracture. In patients with glucocorticoid induced osteoporosis the RANKL/OPG ratio was higher. In patients with chronic obstructive pulmonary disease with low bone mineral density (BMD), RANKL/OPG ratio was significantly higher compared to those with normal BMD. Patients with juvenile idiopathic arthritis had significantly lower levels of OPG in serum and lower OPG/RANKL ratio. The OPG/RANKL/RANK system affects the cardiovascular system as well. In patients with ischemic heart disease the serum concentration of OPG was higher than that of healthy people. In patients with high OPG the risk of cardiovascular mortality is three- or four-times higher than it is in the healthy population. Finally, the presence of malignant tumors leads to an inhibition of OPG production resulting in high bone resorption. The OPG/RANKL/RANK system affects bone loss in many pathological states and participates in pathogenesis of vascular diseases. Determination of OPG concentration or RANKL/OPG ratio is a clinical indicator in the diagnosis of the pathological states mentioned below. Clinical use and areas of investigation: Postmenopausal and glucocorticoid induced osteoporosis, Reumatoid arthritis, juvenile idiopathic arthritis, Ischemic heart disease, Diseases with changed bone resorption activity

Scientific information:

Scientific info:

Osteoprotegerin (OPG, osteoclastogenesis inhibitory factor, OCIF) is a product of the TNFRSF11B gene, located on chromosome 8q24. OPG belongs to the TNF (tumor necrosis factor receptor) superfamily, that plays a key role in bone remodeling. Human OPG is a secreted glycoprotein composed of 401 aminoacid residues. OPG exists as a disulfidelinked homodimer (120 kDa) or as a monomer (60 kDa). Both of these forms are active but the dimer is more bioactive than the monomer. In contrast to most members of the TNF receptor superfamily, OPG probably exists only in a soluble form. Its ligands are RANKL and TRAIL. Human OPG shares 85% aminoacid identity to mouse OPG and 86 % identity to rat OPG. In adult humans OPG mRNA is highly expressed in bones (osteblasts), endothelial vessel cells, skin, liver, stomach, intestine, heart, brain and lung and is also present in atherosclerotic plaques. OPG and RANKL are involved in bone resorption and bone formation. OPG and receptor RANK compete with each other for binding to the ligand RANKL. Binding of RANKL to RANK stimulates osteoclasts and their activity. When RANKL binds to OPG, osteoclastogenesis decreases. OPG prevents the formation of RANKL/RANK, inhibits formation of osteoclasts and suppress bone resorption. At normal physiological conditions OPG and ligand RANKL are in balance and bone resorption and bone formation are linked. This balance can be disrupted by the lack of estrogens in menopausal women, by anti-inflammatory effect of cytokines and by changes in the level of glucocorticoids, thyroid hormones, parathyroid hormone or calcitriol. Any modification in the RANKL/OPG ratio can induce either excessive bone resorption or, in contrast, excessive bone formation. This disregulation can lead to pathological conditions such as osteoporosis/osteopenia, bone tumor associated osteolysis, or cardiovascular pathology. In postmenopausal osteoporosis, OPG serum level decreases and this decrease can be an indicator of a higher risk for bones fracture. In patients with glucocorticoid induced osteoporosis the RANKL/OPG ratio was higher. In patients with chronic obstructive pulmonary disease with low bone mineral density (BMD), RANKL/OPG ratio was significantly higher compared to those with normal BMD. Patients with juvenile idiopathic arthritis had significantly lower levels of OPG in serum and lower OPG/RANKL ratio. The OPG/RANKL/RANK system affects the cardiovascular system as well. In patients with ischemic heart disease the serum concentration of OPG was higher than that of healthy people. In patients with high OPG the risk of cardiovascular mortality is three- or four-times higher than it is in the healthy population. Finally, the presence of malignant tumors leads to an inhibition of OPG production resulting in high bone resorption. The OPG/RANKL/RANK system affects bone loss in many pathological states and participates in pathogenesis of vascular diseases. Determination of OPG concentration or RANKL/OPG ratio is a clinical indicator in the diagnosis of the pathological states mentioned below. Clinical use and areas of investigation: Postmenopausal and glucocorticoid induced osteoporosis, Reumatoid arthritis, juvenile idiopathic arthritis, Ischemic heart disease, Diseases with changed bone resorption activity

Additional information:
Synonyms:	RD194003200; BioVendor

Abd El Dayem S M, Anwar G M, Salama H, Kamel A F, Emara N. Bone mineral density, bone turnover markers, lean mass, and fat mass in Egyptian children with congenital adrenal, hyperplasia. Arch Med Sci. 2010 Jan,:104-110

AbdAllah N, Galal A, Hamed HM, Adolf S, Ragab SH, Abd El Mawgoud S, Rasheed MA. The Roles of Osteoprotegerin and Rankl in Pathogenesis of Osteoporosis in Egyptian Beta Thalassemia Major Patients. Journal of Applied Sciences Re. 2010,6(8): 937-942

Abdel-Hameed RE, Badr HW, Abdallah AA, Hanna WM, Salah N. Osteoporosis in diabetic children. Journal of American Science. 2010,6(12)

Albu A, Fodor D, Bondor C, Craciun AM. Bone metabolism regulators and arterial stiffness in postmenopausal women. Maturitas. 2013 Oct,76 (2):146-50

Avbersek-Luznik I, Balon BP, Rus I, Marc J. Increased bone resorption in HD patients: is it caused by elevated RANKL synthesis?. Nephrol Dial Transplant. 2005 Mar,20 (3):566-70

Avignon A, Sultan A, Piot C, Elaerts S, Cristol JP, Dupuy AM. Osteoprotegerin is associated with silent coronary artery disease in high-risk but asymptomatic type 2 diabetic patients. Diabetes Care. 2005 Sep,28 (9):2176-80

Avignon A, Sultan A, Piot C, Mariano-Goulart D, Thuan Dit Dieudonne JF, Cristol JP, Dupuy AM. Osteoprotegerin: a novel independent marker for silent myocardial ischemia in asymptomatic diabetic patients. Diabetes Care. 2007 Nov,30 (11):2934-9

Barbagallo I, Vanella A, Peterson SJ, Kim DH, Tibullo D, Giallongo C, Vanella L, Parrinello N, Palumbo GA, Di Raimondo F, Abraham NG, Asprinio D. Overexpression of heme oxygenase-1 increases human osteoblast stem cell differentiation. J Bone Miner Metab. 2010 May,28 (3):276-88

Bargnoux AS, Dupuy AM, Garrigue V, Deleuze S, Cristol JP, Mourad G. Renal transplantation decreases osteoprotegerin levels. Transplant Proc. 2006 Sep,38 (7):2317-8

Boyapati A, Msihid J, Fiore S, van Adelsberg J, Graham NM, Hamilton JD. Sarilumab plus methotrexate suppresses circulating biomarkers of bone resorption and synovial damage in patients with rheumatoid arthritis and inadequate response to methotrexate: a biomarker study of MOBILITY. Arthritis Res Ther. 2016 Oct 6,18 (1):225

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Osteoprotegerin Human ELISA

Product specifications for - Osteoprotegerin Human ELISA